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Transcriptional programming of dendritic cells for enhanced MHC class II antigen presentation.

Abstract：

:CD11b(+) dendritic cells (DCs) seem to be specialized for presenting antigens via major histocompatibility (MHC) class II complexes to stimulate helper T cells, but the genetic and regulatory basis for this is not established. Conditional deletion of Irf4 resulted in loss of CD11b(+) DCs, impaired formation of peptide-MHC class II complexes and defective priming of helper T cells but not of cytotoxic T lymphocyte (CTL) responses. Gene expression and chromatin immunoprecipitation followed by deep sequencing (ChIP-Seq) analyses delineated an IRF4-dependent regulatory module that programs enhanced MHC class II antigen presentation. Expression of the transcription factor IRF4 but not of IRF8 restored the ability of IRF4-deficient DCs to efficiently process and present antigen to MHC class II-restricted T cells and promote helper T cell responses. We propose that the evolutionary divergence of IRF4 and IRF8 facilitated the specialization of DC subsets for distinct modes of antigen presentation and priming of helper T cell versus CTL responses.

journal_name

Nat Immunol

journal_title

Nature immunology

authors

Vander Lugt B,Khan AA,Hackney JA,Agrawal S,Lesch J,Zhou M,Lee WP,Park S,Xu M,DeVoss J,Spooner CJ,Chalouni C,Delamarre L,Mellman I,Singh H

doi

10.1038/ni.2795

subject

Has Abstract

pub_date

2014-02-01 00:00:00

pages

161-7

issue

2

eissn

1529-2908

issn

1529-2916

pii

ni.2795

journal_volume

15

pub_type

杂志文章

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